When children with asthma get the flu, they often land in the hospital gasping for air. Researchers at Children's Hospital Boston and collaborating institutions have found a previously unknown biological pathway explaining why influenza induces asthma attacks. Studies in a mouse model, published online on May 29, 2011 by the journal Nature Immunology, reveal that influenza activates a newly recognized group of immune cells called natural helper cells – presenting a completely new set of drug targets for asthma. If activation of these cells, or their asthma-inducing secretions, could be blocked, asthmatic children could be more effectively protected when they get the flu and possibly other viral infections, says senior investigator Dr. Dale Umetsu, of Children's Division of Immunology. Although most asthma is allergic in nature, attacks triggered by viral infection tend to be what put children in the hospital, reflecting the fact that this type of asthma isn't well controlled by existing drugs. "Virtually 100 percent of asthmatics get worse with a viral infection," says Dr. Umetsu. "We really didn't know how that happened, but now we have an explanation, at least for influenza." Natural helper cells were first, very recently, discovered in the intestines and are recognized to play a role in fighting parasitic worm infections as part of the innate immune system (our first line of immune defense). "Since the lung is related to the gut – both are exposed to the environment – we asked if natural helper cells might also be in the lung and be important in asthma," Dr. Umetsu says. Subsequent experiments, led by first authors Drs. Ya-Jen Chang and Hye Young Kim in Dr. Umetsu's lab, showed that the cells are indeed in the lung in a mouse model of influenza-induced asthma, but not in allergic asthma.

Pre-implantation genetic diagnosis (PGD) can give women at risk of passing on a mitochondrial DNA disorder to their offspring a good chance of being able to give birth to an unaffected child, a researcher told the annual conference of the European Society of Human Genetics on May 30, 2011. Dr. Debby Hellebrekers, from Maastricht University Medical Centre, Maastricht, The Netherlands, said that the scientists' findings could have a considerable effect on preventing the transmission of mitochondrial diseases. Mitochondria are cellular organelles involved in the conversion of the energy of food molecules into ATP, the molecule that powers most cellular functions. Disruptions of this energy-producing process, due to a defect in the mitochondrial DNA (mtDNA) or nuclear genes, can cause mitochondrial disorders which represent the most common group of inborn errors of metabolism. The manifestation of mtDNA disorders can be quite varied, but the diseases are almost always serious and, if they do not lead to death, they can result in life-long serious disability for children born with them. Symptoms of mtDNA disorders include loss of muscle co-ordination, visual and hearing problems, poor growth, mental retardation, heart, liver, and kidney disease, neurological problems, respiratory disorders, and dementia. Prenatal diagnosis is in general not possible for mtDNA diseases, because the clinical signs cannot be reliably predicted from the mutation load (the relative amount of mutated mtDNA molecules) in chorionic villus sampling, so the team of scientists from The Netherlands, Australia, and the UK decided to look at whether PGD would be a better alternative. "If we could find a minimal level of mtDNA mutation load below which the chance for an embryo of being affected was acceptably low," said Dr.